The mouse cellular homolog (c-mos) of the Moloney murine sarcoma virus (MSV) transforming sequence (v-mos-Mo) can be activated by linking it to MSV, long-terminal-repeat (LTR) sequences. The human cellular homolog (c-mos-Hu) of mos does not transform even when linked to LTR sequences. Certain recombinants between c-mos-Hu and v-mos which contain sequences derived from both parents, are able to transform NIH 3T3 cells following DNA transfections, but at reduced efficiencies relative to v-mos. Active recombinants containing the 3' portion of c-mos-Hu express high levels of mos protein product, which can be detected by peptide antisera specific for the carboxy-terminus of c-mos-Hu. The pattern of activity observed in c-mos-Hu/v-mos recombinants is consistent with the presence of several functional domains within mos. In c-mos-Hu two of these appear to interact to prevent the expression of a transforming potential. A dominant ras-K gene isolated from the human pancreatic carcinoma cell line, PANC-1, contains a G-A transitional mutation within the 12th codon of the coding sequence. The active ras-K gene encodes an aspartic acid rather than a glycine at position 12. An activated ras-N has also been identified in DNA obtained from a gastric adenocarcinoma. The gene has been cloned from the primary human tumor and the activating lesion localized within the first two coding exons.